ライフサイエンスコーパス: glycogen

1 y biological roles of glycosylation enzymes (glycogenes).

2 exercise-induced IL-6 by maintaining muscle glycogen.

3 elicit similar repletion of IMCLs and muscle glycogen.

4 ie soon after birth and have reduced hepatic glycogen.

5 (mixed-model analysis): P = 0.45] and muscle glycogen (+10.9 +/- 0.9 compared with +12.3 +/- 1.9 mmol

6 V and ADV-treated HK-2 cells had accumulated glycogen, a phenotype that was also observed in mice tre

7 We find that glycogen accumulated on high dietary glucose limits C. e

8 l temperatures due to conditions that favour glycogen accumulating organisms (GAOs) over polyphosphat

9 In fasted double knock-out mice, glycogen accumulation in skeletal and cardiac muscles wa

10 wever, alteration of glycogen metabolism and glycogen accumulation in the brain contributes to neurod

11 in mitochondrial function leads to extensive glycogen accumulation late in oogenesis and is required

12 The resulting glycogen accumulation may partially contribute to TFV an

13 Glycogen accumulation requires prior cellular uptake of

14 These experiments showed that glycogen accumulation was significantly lower in hepatoc

15 The cyclic pattern of glycogen accumulation, an emergent property of the model

16 ochondrial abundance and oxidative capacity, glycogen accumulation, and acquisition of a clear cell p

17 irectly, to compromised sugar catabolism, to glycogen accumulation, and to distorted cell division.

18 ibited severe kidney injury characterized by glycogen accumulation, inflammation, apoptosis, cyst for

19 cterized by left ventricular hypertrophy and glycogen accumulation, with close parallels to mice and

20 r, these effects were independent of cardiac glycogen accumulation.

21 nds directly show a decrease in the level of glycogen and an increase in the levels of fatty acids in

22 istration of exogenous ORM1 increased muscle glycogen and enhanced muscle endurance, whereas ORM1 def

23 After assessment of glycogen and IMCL concentrations in vastus muscles, subj

24 andial metabolism was assessed over 6 h, and glycogen and IMCL concentrations were measured again aft

25 viding carbohydrate and fat as precursors of glycogen and intramyocellular lipid (IMCL) synthesis.

26 Brain glycogen and its metabolism are increasingly recognized

27 hemistry to provide a comparison between the glycogen and lactate distribution revealed by FTIR and t

28 ve method to simultaneously image both brain glycogen and lactate in the same tissue section would be

29 aneous direct spectroscopic imaging of brain glycogen and lactate, in situ within ex vivo tissue sect

30 effect of feeding different carbohydrates on glycogen and lipid biosynthesis in diapausing mosquitoes

31 usively on glucose show accumulation of both glycogen and lipid with increased aliphatic chain length

32 ide and fructose carbon storage into hepatic glycogen and lipids.

33 ved from ingested carbohydrate, stored liver glycogen and newly synthesized glucose (gluconeogenesis)

34 yrophosphorylase (AGPase) controls bacterial glycogen and plant starch biosynthetic pathways, the mos

35 e roles of energy storage molecules, such as glycogen and polyhydroxybutyrate (PHB), in maintaining t

36 ons in synthesis of carbon storage molecules glycogen and polyhydroxybutyrate (PHB).

37 terized by fasting hypoglycaemia and hepatic glycogen and triglyceride overaccumulation.

38 Glucose released from glycogen and used for NADPH/glutathione reduction render

39 e observation of a nonrandom distribution of glycogen, and led us to develop tools to quantitatively

40 Our results establish skeletal muscle glycogen as the source of TCA cycle expansion that norma

41 ing insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling.

42 bunit (Phka1) mRNAs, along with those of the glycogen branching enzyme (GBE) and the phosphorylase b

43 ficantly downregulated and the levels of the glycogen branching enzyme (Gbe1) and muscle-type PhKalph

44 , i.e. glycogen debranching and/or lysosomal glycogen breakdown, contributes to residual glucose prod

45 ive substrate availability caused by blocked glycogen breakdown, the latter because of intrinsic resp

46 and allows CNO-dependent cAMP signaling and glycogen breakdown.

47 e liver of females compare to males, and the glycogen cellular reserves also appeared to decrease mor

48 s to develop tools to quantitatively analyze glycogen clustering and proximity to other subcellular f

49 s upregulated glycolysis, lactate efflux and glycogen content and decreased fatty acid oxidation rate

50 ogenolysis was associated with lower hepatic glycogen content before the onset of exercise and prompt

51 al and cardiac muscles was not affected, but glycogen content in liver was reduced by nearly 73% at 3

52 e correlated with a significant increment of glycogen content in vivo The crystal structure of EcAGPa

53 anterior muscle decreased glucose uptake and glycogen content in vivo, concomitant with decreased abu

54 eased translucency of lysosomes, while total glycogen content remained unchanged.

55 knock-out mice restored the liver lysosomal glycogen content to the level of GAA knock-out mice, as

56 Hepatic glycogen content was approximately 50% greater, glycogen

57 When hepatic glycogen content was lowered, glucagon and NHGO response

58 In Keap1MuKO mice, muscle glycogen content was strongly reduced and forced GBE exp

59 en was significantly impaired, total hepatic glycogen content was substantially decreased, and mice l

60 ), reduced carnitine transporter protein and glycogen content, and increased pyruvate dehydrogenase k

61 Endometrial glycogen content, litter size and weight of offspring at

62 rregulatory axis that is responsive to liver glycogen content.

63 responses that resulted from increased liver glycogen content.

64 early pregnancy, is the rise in endometrial glycogen content.

65 red to the control, whereas soleus and liver glycogen contents were less (P < 0.01 and P < 0.01, resp

66 lization, glycerol release, triglyceride and glycogen contents, free fatty acid (FFA) content and rel

67 Glycogens coupled to the nitrogen atom (N-linked) of asp

68 e show that alpha-glucosidase activity, i.e. glycogen debranching and/or lysosomal glycogen breakdown

69 upled to the release of free glucose through glycogen debranching.

70 sociated with massive liver enlargement from glycogen deposition in children with poorly controlled t

71 and mitochondria and increased collagen and glycogen deposition in TG mice.

72 s and humans, is critical for RNA synthesis, glycogen deposition, and many other essential cellular p

73 ate transporter and characterized by altered glycogen/glucose homeostasis.

74 (LGSKO) that almost completely lacks hepatic glycogen, has impaired glucose disposal, and is pre-disp

75 In fasting conditions, glycogen hepatic levels were further reduced by 84% with

76 hepatic steatosis and disruption of glucose-glycogen homeostasis, leading to hyperglycemia.

77 a surprising function of CD36 in regulating glycogen homeostasis.

78 The concomitant loss of liver glycogen impaired whole-body glucose homeostasis and inc

79 could confer distinct metabolic functions of glycogen in brain.

80 ted with accumulation of residual bodies and glycogen in hearts of 60-week-old knockin mice.

81 ver, these mice were able to mobilize stored glycogen in response to glucagon.

82 his study investigated how the lack of liver glycogen increases fat accumulation and the development

83 Moreover, glycogen interferes with low insulin signalling and acce

84 A small portion of cellular glycogen is transported to and degraded in lysosomes by

85 A) in mammals, but it is unclear why and how glycogen is transported to the lysosomes.

86 /Akt1 mediated inhibitory phosphorylation of glycogen kinase 3beta (GSK3beta) and a subsequent beta-t

87 the collected specimens were used to detect glycogen, lactate, and pH for determining pathogen infec

88 d blood glucose levels but increases hepatic glycogen levels during the daytime or upon fasting.

89 After hepatic glycogen levels were increased, animals underwent a 2-ho

90 in bee bread were correlated with decreased glycogen, lipid, and protein in workers.

91 phosphate pathway, nucleobases, UDP-sugars, glycogen, lipids, and proteins in mouse tissues during 1

92 aracterized by germline-dependent shrinking, glycogen loss, and ectopic vitellogenin expression, util

93 However, alteration of glycogen metabolism and glycogen accumulation in the bra

94 proves that the effect of a mutant enzyme of glycogen metabolism can combine with hyperglycemia to di

95 that brain glycogen phosphorylase (bGP) and glycogen metabolism could be altered by DTCs.

96 We provide evidence that bacterial glycogen metabolism enzymes are secreted into the vacuol

97 Given the key role of glycogen metabolism in brain functions and neurodegenera

98 -time analysis of hepatic glucose fluxes and glycogen metabolism in L-G6pc(-/-) mice using state-of-t

99 indicate that Nrf2 differentially regulates glycogen metabolism in SkM and the liver.

100 re is increasing evidence that alteration of glycogen metabolism in the brain contributes to neurodeg

101 Moreover, alteration of glycogen metabolism in the brain contributes to neurodeg

102 t 3B), encodes a protein (GL) that regulates glycogen metabolism in the liver.

103 onary conservation, our results suggest that glycogen metabolism might also have a role in mammalian

104 Brain glycogen metabolism plays a critical role in major brain

105 bryonic development, cell cycle progression, glycogen metabolism, and immune regulation; deregulation

106 Glycogen phosphorylase (GP), a key enzyme in glycogen metabolism, catalyzes the rate-limiting step of

107 d elusive despite its critical role in brain glycogen metabolism.

108 fic regulation of glycogen phosphorylase and glycogen metabolism.

109 abolism, catalyzes the rate-limiting step of glycogen mobilization.

110 al short chain fatty acids (SCFA), and liver glycogen of triplicate groups of 20 red hybrid tilapia (

111 her compared with histochemical detection of glycogen on the adjacent tissue sections.

112 h suggestive features in whom mitochondrial, glycogen, or lysosomal storage disorders have been exclu

113 ,N-diethyldithiocarbamate suggest that brain glycogen phosphorylase (bGP) and glycogen metabolism cou

114 specific reactive cysteine residues in brain glycogen phosphorylase (bGP).

115 Glycogen phosphorylase (GP), a key enzyme in glycogen me

116 ibitors against muscle and liver isoforms of glycogen phosphorylase (GP).

117 nolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate carbo

118 hase activity was approximately 50% greater, glycogen phosphorylase activity was approximately 50% lo

119 light on the isoform-specific regulation of glycogen phosphorylase and glycogen metabolism.

120 sought to determine whether plasma levels of glycogen phosphorylase BB (GPBB) isoform increased in pa

121 It also showed increased glycogen phosphorylase flux in L-G6pc(-/-) mice, which i

122 Glycogen phosphorylase is the key enzyme that breaks dow

123 a mutation in the catalytic subunit of liver glycogen phosphorylase kinase in a patient with Mauriac

124 e patient's mother possessed the same mutant glycogen phosphorylase kinase subunit, but did not have

125 blood glucose levels physiologically inhibit glycogen phosphorylase to diminish glucose release from

126 with hyperglycemia to directly hyperinhibit glycogen phosphorylase, in turn blocking glycogenolysis

127 iabetic properties due to enzyme inhibition (glycogen phosphorylase, protein tyrosine phosphatase 1B)

128 erent partition of energy stored as IMCLs or glycogen postexercise.The purpose of this study was to c

129 FA, triglycerides, and cholesterol), whereas glycogen production was comparatively low.

130 that the experimental evolution of maternal glycogen provisioning underlies adaptation to a fluctuat

131 experienced normoxia and to decrease embryo glycogen provisioning when they experienced anoxia.

132 dites evolved the ability to increase embryo glycogen provisioning when they experienced normoxia and

133 GSK-3beta is perhaps best known for glycogen regulation, being inhibited downstream in an in

134 metabolic pathway(s) associated with hepatic glycogen repletion.

135 en endogenous glucose storage in the form of glycogen, resistance to oxidative stress and organismal

136 The distribution of glycogen revealed by FTIR spectroscopic imaging has been

137 ) is histologically defined by its lipid and glycogen-rich cytoplasmic deposits.

138 k2p in yeast, as critical for regulating the glycogen shunt flux.

139 muscle and brain that demonstrates that the glycogen shunt functions to maintain homeostasis of glyc

140 The novel role proposed for the glycogen shunt implicates the high activities of glycoge

141 Similarities between the glycogen shunt in yeast and cancer cells lead us here to

142 Loss of the glycogen shunt leads to cell death under substrate stres

143 We propose that the glycogen shunt, a pathway recently shown to be critical

144 lesterol and triglycerides, as well as liver glycogen, significantly increased.

145 - 0.8 vs. 3.2 +/- 0.3 mg kg(-1) min(-1)) and glycogen storage (4.7 +/- 0.6 vs. 2.9 +/- 0.3 mg kg(-1)

146 c overexpression of Ppp1r3b enhanced hepatic glycogen storage above that of controls and, as a result

147 to maintain circadian homeostasis of hepatic glycogen storage and blood glucose levels.

148 se deficiency and characterized by extensive glycogen storage and impaired autophagy.

149 Cell therapy was also found to improve liver glycogen storage and sera glucose level in mice expressi

150 Cell size, protein synthesis, and fat and glycogen storage are repressed by ATXN2 via mTORC1 signa

151 phthalmic findings of a patient with type Ia glycogen storage disease (GSD Ia), DiGeorge syndrome (DG

152 It is a long-standing enigma how glycogen storage disease (GSD) type I patients retain a

153 orn error of metabolism classified as both a glycogen storage disease and a congenital disorder of gl

154 Glycogen storage disease type 1b (GSD-1b) is an autosoma

155 Glycogen storage disease type Ia (GSD-Ia) is characteriz

156 Glycogen storage disease type Ia (GSDIa, von Gierke dise

157 Glycogen storage disease type-Ib (GSD-Ib), deficient in

158 SDIa, von Gierke disease) is the most common glycogen storage disorder.

159 hanced, consistent with elevations in muscle glycogen storage in mice receiving corticosterone.

160 riability, central/internal nuclei, abnormal glycogen storage, presence of autophagic vacuoles and se

161 rage and uptake, ICG uptake and release, and glycogen storage.

162 tic inhibition of glycogen synthase depletes glycogen stores and extends the lifespan of animals fed

163 major role for Ppp1r3b in regulating hepatic glycogen stores and whole-body glucose/energy homeostasi

164 mechanism establishing adequate endometrial glycogen stores for pregnancy.

165 We reveal that host glycogen stores shift to the vacuole through two pathway

166 link intrinsic regulation of glycolysis and glycogen stores to the resolution of neutrophil-mediated

167 occus stops growing, derives energy from its glycogen stores, and greatly decreases rates of macromol

168 normalizes blood glucose levels, dissipates glycogen stores, increases autophagy and restores beta-c

169 ormance, presumably because of lower hepatic glycogen stores.

170 endent upon increases in glycolytic flux and glycogen stores.

171 e widely conserved in plant SS and bacterial glycogen synthase (GS) isoforms.

172 ates insulin and catecholamine signaling and glycogen synthase activity in skeletal muscle.

173 sensitivity was not associated with enhanced glycogen synthase activity or proximal insulin signaling

174 cogen content was approximately 50% greater, glycogen synthase activity was approximately 50% greater

175 Insulin-stimulated glycogen synthase activity was completely ablated during

176 rylation of TBC1D4 Ser(318) and Ser(704) and glycogen synthase activity were greater in the exercised

177 or cell cycle transit as well as controlling glycogen synthase activity.

178 e and phosphorylation of inhibiting sites on glycogen synthase all increased.

179 ogen shunt implicates the high activities of glycogen synthase and fructose bisphosphatase in tumors

180 Firstly, the periportal zonation of both glycogen synthase and the oxidative phosphorylation enzy

181 levels of oxidants or genetic inhibition of glycogen synthase depletes glycogen stores and extends t

182 Moreover, glycogen synthase expression was greatly enhanced, consi

183 the Gys2 gene encoding the liver isoform of glycogen synthase generates a mouse strain (LGSKO) that

184 They activate glycogen synthase in insulin receptor-expressing CHO-IR

185 lecular signaling at the level of TBC1D4 and glycogen synthase in muscle.

186 Glycogen synthase kinase (GSK)-3 is a ubiquitously expre

187 Blast TBI increased glycogen synthase kinase (GSK)-3beta activities in ApoE4

188 These same stimuli enhance glycogen synthase kinase (GSK)-3beta activity through in

189 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het

190 Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyp

191 used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot

192 Here we show that glycogen synthase kinase 3 (GSK-3) interacts with and ph

193 Glycogen synthase kinase 3 (GSK-3, isoforms alpha and be

194 Here we show how inhibiting glycogen synthase kinase 3 (GSK3) can improve the differ

195 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona

196 Herein, we investigated the role of glycogen synthase kinase 3 (GSK3) in liver regeneration

197 Here we show that glycogen synthase kinase 3 (Gsk3) is a metabolic sensor

198 Here, we show the expression of the Glycogen synthase kinase 3 (GSK3) MoGSK1 in M. oryzae is

199 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm

200 Glycogen synthase kinase 3 (GSK3) plays a central role i

201 mine analogues which are inhibitors of human glycogen synthase kinase 3 (GSK3).

202 mitochondrial respiratory quiescence through glycogen synthase kinase 3 (GSK3).

203 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o

204 Glycogen synthase kinase 3 beta (GSK-3beta) is a central

205 The BCR attenuates glycogen synthase kinase 3 beta (GSK3beta) activity to s

206 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f

207 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific

208 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas

209 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r

210 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti

211 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s

212 A member of this family is glycogen synthase kinase 3beta (GSK3beta) interaction pr

213 We show that glycogen synthase kinase 3beta (GSK3beta) interacts with

214 Glycogen synthase kinase 3beta (GSK3beta) is a constitut

215 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio

216 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path

217 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l

218 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major

219 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p

220 The phosphorylation is catalyzed by glycogen synthase kinase 3beta (GSK3beta), ultimately re

221 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi

222 PI exposure abrogated glycogen synthase kinase 3beta (GSK3beta)-mediated degra

223 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k

224 t VRK2 activity was negatively controlled by glycogen synthase kinase 3beta (GSK3beta).

225 n (mTOR) signaling pathway and inhibition of glycogen synthase kinase 3beta (GSK3beta).

226 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin

227 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i

228 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression

229 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o

230 Molecularly, ROCK inhibition induced glycogen synthase kinase 3beta-dependent phosphorylation

231 ta-catenin expression and stabilization in a glycogen synthase kinase 3beta-independent manner.

232 7, p38 mitogen-activated protein kinase, and glycogen synthase kinase 3beta.

233 A point mutation in a putative glycogen synthase kinase phosophorylation site within th

234 lates alcohol-induced BK internalization via glycogen synthase kinase phosphorylation.

235 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith

236 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central

237 Glycogen synthase kinase-3 (GSK-3) is a constitutively a

238 Glycogen synthase kinase-3 (GSK-3) regulates multiple ce

239 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e

240 Predictably, inhibition of glycogen synthase kinase-3 (GSK-3), which results from a

241 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap

242 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin

243 The glycogen synthase kinase-3 (GSK3) family kinases are cen

244 Treatment with lithium or a glycogen synthase kinase-3 (GSK3) inhibitor corrects beh

245 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru

246 Moreover, induction of glycogen synthase kinase-3 (GSK3) performed using a Wnt

247 Glycogen synthase kinase-3 (GSK3) regulates many physiol

248 Pharmacological inhibition of glycogen synthase kinase-3 was sufficient to reverse the

249 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,

250 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking

251 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could

252 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa

253 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati

254 hase and the phosphorylation (inhibition) of glycogen synthase kinase-3beta (GSK-3beta).

255 hase and the phosphorylation (inhibition) of glycogen synthase kinase-3beta (GSK-3beta).

256 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and

257 Glycogen synthase kinase-3beta (GSK3beta) has diverse bi

258 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was

259 tion and insulin secretion via regulation of glycogen synthase kinase-3beta (GSK3beta).

260 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat

261 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa

262 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa

263 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re

264 l as by inhibition of the Akt-GSK-3beta (Akt-glycogen synthase kinase-3beta) pathway.

265 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.

266 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.

267 ntify the Arabidopsis (Arabidopsis thaliana) GLYCOGEN SYNTHASE KINASE3 (GSK3)/Shaggy-like kinase ASKa

268 nt link between phosphoinositol-3-kinase and glycogen synthase kinase3 and demonstrates the potential

269 athway has many downstream targets including glycogen synthase kinase3 which is a major regulatory ki

270 b The Ppp1r3b deletion significantly reduced glycogen synthase protein abundance, and the remaining p

271 50% lower, and the amount of phosphorylated glycogen synthase was 34% lower, indicating activation o

272 ence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor TWS119, and geneticall

273 ast, Zip14 KO mice exhibited greater hepatic glycogen synthesis and impaired gluconeogenesis and glyc

274 such conditions, fructose lowers whole-body glycogen synthesis and impairs subsequent exercise perfo

275 terruptions resulted in greater capacity for glycogen synthesis and likely for ATP production.

276 Our results suggest that loss of liver glycogen synthesis diverts glucose toward fat synthesis,

277 owever certain enzymes in the glycolysis and glycogen synthesis pathway had elevated expression in TF

278 storage (estimating total, muscle, and liver glycogen synthesis) compared with GLU (+117 +/- 9 compar

279 Overexpression of CD36 promoted glycogen synthesis, and as a result, CD36Tg mice were pr

280 able, insulin-independent glucose uptake and glycogen synthesis, with resultant improvements in glyce

281 rrent with glucose uptake and suppression of glycogen synthesis.

282 insulin-stimulated 2-deoxyglucose uptake and glycogen synthesis.

283 muscle glucose uptake and decreased hepatic glycogen synthesis.

284 se inhibition were reliant on glycolysis and glycogen synthesis.

285 m, Akt/PKB; (c) inhibited insulin-stimulated glycogen synthesis; and (d) decreased oxygen consumption

286 (marked by biochemical constituents such as glycogen that are involved in compensatory metabolic mec

287 se infusion caused a large increase in liver glycogen that markedly elevated the response of epinephr

288 e recognised by INCh1 is also a component of glycogen, this mAb can also be used in mammalian systems

289 k-out mice, indicating that the transport of glycogen to lysosomes was suppressed in liver by the los

290 phorylase is the key enzyme that breaks down glycogen to yield glucose-1-phosphate in order to restor

291 ther determine whether Stbd1 participates in glycogen transport to lysosomes, we generated GAA/Stbd1

292 ngly, we observed similar ETC remodeling and glycogen uptake in maturing Xenopus oocytes, suggesting

293 carbohydrate oxidation and muscle and liver glycogen utilization, and reduced whole-body fat oxidati

294 ing the first 4 hours of each study, hepatic glycogen was increased by augmenting hepatic glucose upt

295 sequence, glucose incorporation into hepatic glycogen was significantly impaired, total hepatic glyco

296 Whereas glucose incorporation to glycogen was unaltered by small interfering RNA against

297 found, non-physiological increase in cardiac glycogen, which might abnormally alter the true phenotyp

298 squitoes fed on sucrose primarily accumulate glycogen with increased branching structures, but less o

299 s capacities to store glucose in the form of glycogen, with feeding, and assemble glucose via the glu

300 nt cardiac hypertrophy and increased cardiac glycogen without apparent functional sequelae.